scholarly journals Chronic Esophagitis

2020 ◽  
Author(s):  
Keyword(s):  
Chronic Esophagitis

Radiologic findings in chronic esophagitis dissecans.

1998 ◽  
Vol 170 (6) ◽  
pp. 1671-1672 ◽  
Author(s):  
O Catalano ◽  
G Lapiccirella ◽  
A Nunziata
Keyword(s):  
Radiologic Findings ◽  
Chronic Esophagitis

Roles of epidermal growth factor and Na+/H+ exchanger-1 in esophageal epithelial defense against acid-induced injury

2006 ◽  
Vol 290 (4) ◽  
pp. G665-G673 ◽  
Author(s):  
Yasuhiro Fujiwara ◽  
Kazuhide Higuchi ◽  
Takashi Takashima ◽  
Masaki Hamaguchi ◽  
Tsuyoshi Hayakawa ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial Cells ◽  
Acid Reflux ◽  
Dependent Manner ◽  
Egf Receptors ◽  
Epithelial Proliferation ◽  
Epidermal Growth ◽  
Esophageal Epithelial Cells ◽  
Chronic Esophagitis

Epidermal growth factor (EGF) is predominantly secreted by salivary glands and activates Na+/H+ exchanger-1 (NHE-1), which regulates intracellular pH (pHi). We investigated the roles of EGF and NHE-1 in esophageal epithelial defense against acid using human esophageal epithelial cell lines and a rat chronic esophagitis model. Esophageal epithelial cells were incubated with acidified medium in the absence or presence of EGF. Cell viability and changes in pHi were measured. Chronic acid reflux esophagitis was induced in rats with and without sialoadenectomy. Esophageal lesion index, epithelial proliferation, and expression of EGF receptors and NHE-1 were examined. EGF protected esophageal epithelial cells against acid in a dose-dependent manner, and the cytoprotective effect of EGF was completely blocked by treatment with NHE-1 inhibitors. Tyrosine kinase, calmodulin, and PKC inhibitors significantly inhibited cytoprotection by EGF, whereas MEK, phosphatidylinositol 3-kinase, and PKA inhibitors had no effect. EGF significantly increased pHi recovery after NH4Cl pulse acidification, and this increase in pHi recovery was significantly blocked by inhibitors of calmodulin and PKC. Sialoadenectomy led to an increase in the severity of chronic esophagitis but affected neither epithelial proliferation nor expression of EGF receptors. Expression of NHE-1 mRNA was increased in esophagitis and upregulated in rats with sialoadenectomy. The increasing severity of esophagitis in rats with sialoadenectomy was prevented by exogenous administration of EGF. In conclusion, EGF protects esophageal epithelial cells against acid through NHE activation via Ca2+/calmodulin and the PKC pathway. Deficiency in endogenous EGF is associated with increased severity of esophagitis. EGF and NHE-1 play crucial roles in esophageal epithelial defense against acid.

Treatment of Chronic Esophagitis Dissecans with Swallowed Fluticasone

2006 ◽  
Vol 101 ◽  
pp. S368
Author(s):  
Sunil Patel ◽  
Neil Phelan ◽  
Barbara Banner ◽  
Kanishka Bhattacharya
Keyword(s):  
Chronic Esophagitis

Role of pancreatic trypsin in chronic esophagitis induced by gastroduodenal reflux in rats

2006 ◽  
Vol 41 (3) ◽  
pp. 198-208 ◽  
Author(s):  
Yuji Naito ◽  
Kazuhiko Uchiyama ◽  
Masaaki Kuroda ◽  
Tomohisa Takagi ◽  
Satoshi Kokura ◽  
...  
Keyword(s):  
Chronic Esophagitis

scholarly journals Management of Toxicities of Combined Modality Therapy for Intrathoracic Malignancies

1996 ◽  
Vol 3 (4) ◽  
pp. 329-335 ◽  
Author(s):  
Tina Weakland ◽  
Henry Wagner
Keyword(s):  
Patient Care ◽  
Combined Modality Therapy ◽  
Neurologic Deficits ◽  
Combined Modality ◽  
Management Measures ◽  
Optimal Patient Care ◽  
Chemotherapy Patients ◽  
Management Recommendations ◽  
Chronic Esophagitis

Background Combined radiation and chemotherapy for intrathoracic tumors can produce appreciable morbidity. Apprehension about the severity of these toxicities may inhibit optimal patient care. Methods The literature on recognition, diagnosis, prophylaxis, and management of these toxicities is reviewed and combined with the experiences of the authors to produce management recommendations. Results Toxicities include acute and chronic esophagitis, early and late pneumonitis with fibrosis, myelosuppression, and neurologic deficits. Measures are available to minimize their severity and to reduce their impact on the patient. Conclusions The morbidity of combined radiation and chemotherapy patients with intrathoracic tumors can be minimized by recognizing potential toxicities and by applying appropriate prophylactic and management measures.

Sign in / Sign up

Export Citation Format

Share Document